GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Ghrelin differentially modulates glucose-induced insulin secretion according to feeding status in sheep.
Takahashi. Hideyuki H; Kurose. Yohei Y; Sakaida. Muneyuki M; Suzuki. Yoshihiro Y; Kobayashi. Shigeki S; Sugino. Toshihisa T; Kojima. Masayasu M; Kangawa. Kenji K; Hasegawa. Yoshihisa Y; Terashima. Yoshiaki Y
Key Findings
- Blocking the ghrelin receptor (with D‑Lys3‑GHRP6) increased glucose‑stimulated insulin secretion during fasting.
- Administering synthetic ghrelin during a meal increased glucose‑stimulated insulin secretion.
- The effect of ghrelin on insulin is opposite in fasting vs. fed states, acting through the GHS‑R1a receptor.
Practical Outcomes
- For biohackers, the data suggest that timing matters if you plan to modulate ghrelin (or use GHRP‑6). Blocking ghrelin during a fast might help improve insulin response, while giving a ghrelin agonist around meals could support post‑meal insulin spikes. However, the findings are from sheep and not directly tested in humans, so any protocol would be experimental and should be approached cautiously.
Summary
In sheep, the hormone ghrelin works opposite ways depending on whether the animal is fasting or has just eaten. When fasting, blocking ghrelin makes the pancreas release more insulin in response to glucose. After a meal, giving extra ghrelin boosts insulin release. The study shows ghrelin can both suppress and enhance insulin, depending on feeding status.
Abstract
The present study was conducted to investigate roles of ghrelin in glucose-induced insulin secretion in fasting- and meal-fed state in sheep. Castrated Suffolk rams were fed a maintenance diet of alfalfa hay cubes once a day. Hyperglycemic clamp (HGC) was carried out to examine glucose-induced insulin response from 48 to 53 h (fasting state) and from 3 to 8 h (meal-fed state) after feeding in Experiment 1 and 2 respectively. Total dose of 70 nmol/kg body weight of D-Lys3-GHRP6, a GH secretagogue receptor 1a (GHS-R1a) antagonist, was intravenously administered at 0, 60, and 120 min after the commencement of HGC. In the fasting state, the ghrelin antagonist significantly (P < 0.01) enhanced glucose-induced insulin secretion. In the meal-fed state, i.v. administration of synthetic ovine ghrelin (0.04 microg/kg body weight per min during HGC) significantly (P < 0.05) enhanced glucose-induced insulin secretion. d-Lys3-GHRP6 treatment suppressed ghrelin-induced enhancement of the insulin secretion. In conclusion, ghrelin has an inhibitory and stimulatory role in glucose-induced insulin secretion via GHS-R1a in fasting- and meal-fed state respectively.
Study Information
pubmed
2007
10.1677/joe-07-0206